Erasmus University Rotterdam

About: Erasmus University Rotterdam is a education organization based out in Rotterdam, Zuid-Holland, Netherlands. It is known for research contribution in the topics: Population & Health care. The organization has 35466 authors who have published 91288 publications receiving 4510972 citations. The organization is also known as: EUR.

Pathogenesis and Transmission of Swine-Origin 2009 A(H1N1) Influenza Virus in Ferrets

Abstract: The swine-origin A(H1N1) influenza virus that has emerged in humans in early 2009 has raised concerns about pandemic developments. In a ferret pathogenesis and transmission model, the 2009 A(H1N1) influenza virus was found to be more pathogenic than a seasonal A(H1N1) virus, with more extensive virus replication occurring in the respiratory tract. Replication of seasonal A(H1N1) virus was confined to the nasal cavity of ferrets, but the 2009 A(H1N1) influenza virus also replicated in the trachea, bronchi, and bronchioles. Virus shedding was more abundant from the upper respiratory tract for 2009 A(H1N1) influenza virus as compared with seasonal virus, and transmission via aerosol or respiratory droplets was equally efficient. These data suggest that the 2009 A(H1N1) influenza virus has the ability to persist in the human population, potentially with more severe clinical consequences.

Early-life determinants of overweight and obesity: a review of systematic reviews

Abstract: The aim of this paper was to review the evidence for early-life (from conception to 5 years of age) determinants of obesity. The design is review of published systematic reviews. Data sources included Medline, Embase, Web of Science, Cochrane Library, CINAHL, PsycINFO. Identification of 22 eligible reviews from a database of 12,021 independent publications. Quality of selected reviews assessed using the Assessment of Multiple Systematic Reviews score. Articles published after the reviews were used to confirm results. No review was classified as high quality, 11 as moderate and 11 as low. Factors associated with later overweight and obesity: maternal diabetes, maternal smoking, rapid infant growth, no or short breastfeeding, obesity in infancy, short sleep duration, <30 min of daily physical activity, consumption of sugar-sweetened beverages. Other factors were identified as potentially relevant, although the size of their effect is difficult to estimate. Maternal smoking, breastfeeding, infant size and growth, short sleep duration and television viewing are supported by better-quality reviews. It is difficult to establish a causal association between possible determinants and obesity, and the relative importance of each determinant. Future research should focus on early-life interventions to confirm the role of protective and risk factors and to tackle the high burden obesity represents for present and future generations.

A Unified Theory of Sepsis-Induced Acute Kidney Injury: Inflammation, microcirculatory dysfunction, bioenergetics and the tubular cell adaptation to injury

Abstract: Given that the leading clinical conditions associated with acute kidney injury (AKI), namely, sepsis, major surgery, heart failure, and hypovolemia, are all associated with shock, it is tempting to attribute all AKI to ischemia on the basis of macrohemodynamic changes. However, an increasing body of evidence has suggested that in many patients, AKI can occur in the absence of overt signs of global renal hypoperfusion. Indeed, sepsis-induced AKI can occur in the setting of normal or even increased renal blood flow. Accordingly, renal injury may not be entirely explained solely on the basis of the classic paradigm of hypoperfusion, and thus other mechanisms must come into play. Herein, we put forward a "unifying theory" to explain the interplay between inflammation and oxidative stress, microvascular dysfunction, and the adaptive response of the tubular epithelial cell to the septic insult. We propose that this response is mostly adaptive in origin, that it is driven by mitochondria, and that it ultimately results in and explains the clinical phenotype of sepsis-induced AKI.